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WormBase Tree Display for Variation: WBVar00317467

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Name Class

WBVar00317467NamePublic_nametm5221
Sequence_detailsSMapS_parentSequenceC30C11
Flanking_sequencesttaaataaagttaattaatacacgaatttcataacaataaaattcaagaaataagtcaac
Mapping_targetC30C11
Source_location7CHROMOSOME_III84436798443872Inferred_automaticallyNational_Bioresource_Project
Type_of_mutationDeletion
PCR_producttm5221_external
tm5221_internal
SeqStatusSequenced
Variation_typeAllele
OriginSpeciesCaenorhabditis elegans
LaboratoryFX
AuthorMitani S
DB_infoDatabaseNational_Bioresource_Projectseq5221
NBP_allele
StatusLive
IsolationMutagenTMP/UV
GeneticsMapIII
DescriptionPhenotypeWBPhenotype:0000016Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Remark"...compared to WT animals, all Ufm1 cascade mutants displayed a significantly higher rate of pharynx grinder paralysis in the presence of aldicarb (Figure 3A), pointing to a pathophysiological mechanism involving an increased amount of ACh in the neuromuscular junctions." ACh = acetylcholinePaper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00003650Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_assayControl_strainWBStrain00000001Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
TreatmentAnimals treated with 0.5 mM aldicarb for 60 minutesPaper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
WBPhenotype:0000303Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Remark"In a next step, using a computer-aided chemotaxis assay, we analyzed the effects of the Ufm1 cascade on C. elegans sensorial behavior by a chemotaxis assay with the attractant diacetyl. Results revealed a decreased ability in sensing diacetyl in all mutants compared to WT animals (Figure 3C), pointing to a failure in the C. elegans sensory system in the absence of the Ufm1 cascade and its targets."Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00002819Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_assayControl_strainWBStrain00000001Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
WBPhenotype:0002634Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Remark"In addition, because C. elegans uba-5(ok3364) mutants are resistant to ER stress, we monitored the effect of dithiothreitol (DDT) treatment on all Ufm1 cascade mutants and found that, compared to WT, they were resistant to ER stress (Figure 3B)."Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004908Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_assayControl_strainWBStrain00000001Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Treatment18 hr treatment with the ER-stressor dithiothreitol (DTT, 11 mM),Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_not_observedWBPhenotype:0000062Person_evidenceWBPerson7743
Curator_confirmedWBPerson712
RemarkClassified as homozygous viable by the National Bioresource Project of Japan.Person_evidenceWBPerson7743
Curator_confirmedWBPerson712
WBPhenotype:0000523Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Remark"Wild-type (N2 Bristol) and Ufm1 cascade mutant worms (Table S3) did not show a seizure phenotype in the presence of PTZ, whereas PTZ-sensitive worms (unc-43) showed severe seizure phenotypes (data not shown)." PTZ = pentylenetetrazolePaper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004251Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_assayControl_strainWBStrain00000001Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
TreatmentAnimals were treated with pentylenetetrazolePaper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
WBPhenotype:0000845Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Remark"Treatment with levamisole, an ACh receptor agonist known to paralyze worms, did not induce differences in motility between control and mutant worms (Figure S5), suggesting that the alteration of Ufm1 cascade and of Ufbp1 and Cdkr3 induce increased ACh release in neuromuscular junctions."Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Affected_byMoleculeWBMol:00004019Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Phenotype_assayControl_strainWBStrain00000001Paper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
TreatmentAnimals treated with 0.4 mM levamisole for 3 hoursPaper_evidenceWBPaper00050013
Curator_confirmedWBPerson2987
Disease_infoModels_diseaseDOID:0050709
Models_disease_in_annotationWBDOannot00000814
ReferenceWBPaper00050013
Remark[C30C11] 1196/1197-[C30C11] 1388/1389 (192 bp deletion)
This knockout was generated by the National Bioresource Project, Tokyo, Japan, which is part of the International C. elegans Gene Knockout Consortium, which should be acknowledged in any publications resulting from its use.Paper_evidenceWBPaper00041807
MethodNBP_knockout_allele